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D2 autoreceptors chronically enhance dopamine neuron pacemaker activity.

Junghyun Hahn¹, Paul H M Kullmann, John P Horn

¹Department of Pharmacology, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience

|May 12, 2006

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D2 autoreceptors on dopamine neurons acutely inhibit firing but chronically enhance it by altering A-type K+ channels. This long-term action increases the speed and regularity of neuron firing.

Area of Science:

Neuroscience
Cellular electrophysiology

Background:

D2 autoreceptors on midbrain dopamine neurons acutely inhibit pacemaker activity by opening K+ channels.
The long-term effects of D2 autoreceptor activation on dopamine neuron firing patterns are not well understood.

Purpose of the Study:

To investigate the chronic effects of D2 autoreceptor activation on dopamine neuron firing.
To elucidate the molecular mechanisms underlying the long-term regulation of dopamine neuron activity by D2 autoreceptors.

Main Methods:

Whole-cell and perforated patch-clamp recordings were used to study cultured rat midbrain dopamine neurons.
Voltage-, current-, and dynamic-clamp techniques were employed to analyze neuronal firing properties.
The role of cAMP and protein kinase A in mediating D2 autoreceptor effects was investigated.

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Main Results:

Chronic D2 autoreceptor activation increased the speed and regularity of action potential firing.
Changes in the number of functional A-type K+ channels were found to alter firing rate and susceptibility to irregularity.
cAMP and protein kinase A mediated the long-term effects, countering the acute signaling pathway actions.

Conclusions:

D2 autoreceptors mediate long-term enhancement of dopamine neuron firing rate and fidelity.
These findings reveal a dual role for D2 autoreceptors in regulating dopamine neuron activity, with opposing acute and chronic effects.
The study highlights the importance of A-type K+ channels and cAMP/PKA signaling in the long-term plasticity of dopamine neuron pacemaking.